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  • Title: Betulinic acid induces apoptosis through a direct effect on mitochondria in neuroectodermal tumors.
    Author: Fulda S, Debatin KM.
    Journal: Med Pediatr Oncol; 2000 Dec; 35(6):616-8. PubMed ID: 11107130.
    Abstract:
    BACKGROUND AND PROCEDURE: We identified BetA as a new cytotoxic agent active against neuroectodermal tumor cells including neuroblastoma, medulloblastoma, glioblastoma and Ewing sarcoma cells, representing the most common solid tumors of childhood. RESULTS: BetA induced apoptosis by a direct effect on mitochondria independent of accumulation of wild-type p53 protein and independent of death-inducing ligand/receptor systems such as CD95. Mitochondrial perturbations on treatment with BetA resulted in the release of soluble apoptogenic factors such as cytochrome c or AIF from mitochondria into the cytosol, where they induced activation of caspases. Overexpression of the anti-apoptotic proteins Bcl-2 or Bcl-X(L) that blocked loss of the mitochondrial membrane potential and cytochrome c release from mitochondria also conferred resistance to BetA. Most importantly, BetA exhibited potent antitumor activity on neuroblastoma cells resistant to CD95- or doxorubicin-triggered apoptosis and on primary tumor cells from patients with neuroectodermal tumors. CONCLUSIONS: Thus, BetA may be a promising new agent in the treatment of neuroectodermal tumors including neuroblastoma in vivo.
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